Metabolic effects of hypothalamic hyperphagia.
In order to test the hypothesis that the enhanced gluconeogenesis of hypothalamic obesity remains responsive to changed in food intake, we have measured gluconeogenesis in two modes of hypothalamic obesity under both hyperphagic and normophagic conditions. The results show that hyperphagia partially decreases gluconeogenesis and fully restores liver glycogen in both modes. The discussion section relates our present findings to the enhanced glucose utilization previously noted after VMH destruction and to the recent hypothesis that hyperphagia is a response to body protein depletion.
D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D001068:Feeding and Eating Disorders / Q000503:physiopathology*; D005260:Female; D005943:Gluconeogenesis; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D006963:Hyperphagia / Q000150:complications / Q000503:physiopathology*; D007031:Hypothalamus / Q000502:physiology*; D007033:Hypothalamus, Middle / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D051381:Rats
D002245:Carbon Dioxide; D006003:Glycogen